Overweight is associated with triglyceride accumulation in cardiomyocytes, which can cause cardiac dysfunction. It is also associated with reduced synthesis and plasma concentration of atrial natriuretic peptide (ANP). In adipocytes, ANP stimulates lipolysis through natriuretic peptide receptor-A (NPR-A), leading to cGMP-dependent phosphorylation of hormone-sensitive lipase. Cardiac myocytes express NPR-A and hormone-sensitive lipase. In the present study, we investigated whether ANP affects triglyceride stores in the heart. Subcutaneously implanted osmotic minipumps were used to administer ANP (125 or 500 ng/kg/min) or saline to obese leptin-deficient (ob/ob) mice or lean control mice (ob/+) for a week. ANP (500 ng/kg/min) reduced blood pressure but did not affect the cardiac triglyceride stores or mRNA expression of NPR-A and NPR-C. Also, deficiency of NPR-A did not affect the cardiac triglyceride content. Finally, addition of ANP to the culture medium (10−7 mol/l) increased cellular cGMP content (P=0.009) but did not affect triglyceride stores in HL-1 cardiac myocyte cultures. Hence, ANP does not affect triglyceride stores in the murine heart.
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aDepartment of Clinical Biochemistry, Copenhagen University Hospital Rigshospitalet
bDepartment of Biomedical Science
cDepartment of Clinical Medicine, Faculty of Medical and Health Sciences, University of Copenhagen, Copenhagen, Denmark
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Correspondence to Emil D. Bartels, MD, PhD, Department of Clinical Biochemistry, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark Tel: +45 354 53011; fax: +45 354 52880; e-mail: firstname.lastname@example.org
Received August 27, 2013
Accepted January 9, 2014